Mechanisms of Medial Wall Thinning in Chronic Total Occlusion.

Background: The success rate of percutaneous coronary intervention (PCI) for chronic total occlusion (CTO) is lower and the risk for complications higher compared with other non-CTO PCI. Although interventionalists focus on intimal plaque characteristics, the coronary media is an important (especially for techniques involving antegrade dissection and re-entry) but poorly understood structure in CTO PCI.

Objectives: The aim of the present study was to investigate coronary medial wall thinning in CTO lesions and determine how this thinning might affect CTO PCI.

CD163 Macrophages Induce Endothelial-to-Mesenchymal Transition in Atheroma.

Background: Cell phenotype switching is increasingly being recognized in atherosclerosis. However, our understanding of the exact stimuli for such cellular transformations and their significance for human atherosclerosis is still evolving. Intraplaque hemorrhage is thought to be a major contributor to plaque progression in part by stimulating the influx of CD163 macrophages.

Clonal Proliferation Within Smooth Muscle Cells in Unstable Human Atherosclerotic Lesions.

Background: Studies in humans and mice using the expression of an X-linked gene or lineage tracing, respectively, have suggested that clones of smooth muscle cells (SMCs) exist in human atherosclerotic lesions but are limited by either spatial resolution or translatability of the model.

Methods: Phenotypic clonality can be detected by X-chromosome inactivation patterns. We investigated whether clones of SMCs exist in unstable human atheroma using RNA in situ hybridization (BaseScope) to identify a naturally occurring 24-nucleotide deletion in the 3'UTR of the X-linked (biglycan) gene, a proteoglycan highly expressed by SMCs.

Histologic Assessment of Thromboemboli Due to Plaque Rupture, Plaque Erosion, or COVID-19 Microthrombi.

Plaque rupture, plaque erosion, and COVID-19 infection can cause acute coronary syndromes (ACS). We illustrate case examples demonstrating the distinctive and characteristic pathologic findings underlying each of these various causes of acute myocardial infarction. A deeper understanding of the pathophysiology of ACS is necessary for the development of newer agents and techniques to improve outcomes after ACS.

Local, Downstream, and Systemic Evaluation after Femoral Artery Angioplasty with Kanshas Drug-Coated Balloons In Vitro and in a Healthy Swine Model.

Purpose: To evaluate the incidence of distal embolism and local vascular responses after treatment with the Kanshas drug-coated balloon (DCB) in a preclinical model.

Materials And Methods: A total of 90 femoral arteries from 35 healthy swine were treated with a single-dose (×1) or triple-dose (×3) Kanshas DCB that applies the Unicoat technology with 3.2 μg/mm of paclitaxel.

The histological analysis of the coronary medial thickness: Implications for percutaneous coronary intervention.

Background: A deeper understanding of coronary medial thickness is important for coronary intervention because media thickness can limit the safety and effectiveness of interventional techniques. However, there is a paucity of detailed data on human coronary medial thickness so far.

Materials And Methods: We investigated the thickness of the media by histologic analysis.

Understanding the role of alternative macrophage phenotypes in human atherosclerosis.

Introduction: Atherosclerosis-based ischemic heart disease is still the primary cause of death throughout the world. Over the past decades there has been no significant changes in the therapeutic approaches to atherosclerosis, which are mainly based on lipid lowering therapies and management of comorbid conditions such as diabetes and hypertension. The involvement of macrophages in atherosclerosis has been recognized for decades.

Myeloid-associated lipin-1 transcriptional co-regulatory activity is atheroprotective.

Background And Aims: Atherosclerosis is the most prominent underlying cause of cardiovascular disease (CVD). It is initiated by cholesterol deposition in the arterial intima, which causes macrophage recruitment and proinflammatory responses that promote plaque growth, necrotic core formation, and plaque rupture. Lipin-1 is a phosphatidic acid phosphohydrolase for glycerolipid synthesis.

AAV8-mediated overexpression of mPCSK9 in liver differs between male and female mice.

Background And Aims: The recombinant adeno-associated viral vector serotype 8 expressing the gain-of-function mutation of mouse proprotein convertase subtilisin/kexin type 9 (AAV8- PCSK9) is a new model for the induction of hypercholesterolemia. AAV8 preferentially infects hepatocytes and the incorporated liver-specific promoter should ensure expression of PCSK9 in the liver. Since tissue distribution of AAVs can differ between male and female mice, we investigated the differences in PCSK9 expression and hypercholesterolemia development between male and female mice using the AAV8-PCSK9 model.

Absence of Nicotinamide Nucleotide Transhydrogenase in C57BL/6J Mice Exacerbates Experimental Atherosclerosis.

Background: Mitochondrial reactive oxygen species (ROS) contribute to inflammation and vascular remodeling during atherosclerotic plaque formation. C57BL/6N (6N) and C57BL/6J (6J) mice display distinct mitochondrial redox balance due to the absence of nicotinamide nucleotide transhydrogenase (NNT) in 6J mice. We hypothesize that differential NNT expression between these animals alters plaque development.

Macrophage-Associated Lipin-1 Enzymatic Activity Contributes to Modified Low-Density Lipoprotein-Induced Proinflammatory Signaling and Atherosclerosis.

Objective: Macrophage proinflammatory responses induced by modified low-density lipoproteins (modLDL) contribute to atherosclerotic progression. How modLDL causes macrophages to become proinflammatory is still enigmatic. Macrophage foam cell formation induced by modLDL requires glycerolipid synthesis.

Lipin-1 contributes to modified low-density lipoprotein-elicited macrophage pro-inflammatory responses.

Atherosclerosis is a chronic inflammatory disease of large and medium-sized arteries and the underlying cause of cardiovascular disease, a major cause of mortality worldwide. The over-accumulation of modified cholesterol-containing low-density lipoproteins (e.g.

Natural killer T (NKT) cells accelerate Shiga toxin type 2 (Stx2) pathology in mice.

Shiga toxin-producing Escherichia coli (STEC) is a leading cause of childhood renal disease Hemolytic Uremic Syndrome (HUS). The involvement of renal cytokines and chemokines is suspected to play a critical role in disease progression. In current article, we tested the hypothesis that NKT cells are involved in Stx2-induced pathology in vivo.